ACTG 368 - Viral replication can be successfully suppressed in nucleoside analog-experienced patients with advanced HIV-infection using the substitution of potent new agents including indinavir sulfate (IDV, a protease inhibitor); DMP-266 (a non-nucleoside reverse transcriptase inhibitor [NNRTI]) currently being studied in combination with IDV; and 1592U89 (a nucleoside analog reverse transcriptase inhibitor). The hypothesis of this study is that combinations of alternative, potent agents will still succeed in this circumstance but it is unclear whether it is best to add a new nucleoside analog, a new NNRTI, or both to a protease inhibitor to achieve plasma HIV RNA levels which are below the limits of detection. The three-arm, placebo controlled design of this study will permit determination of the relative contributions of 1592U89, (2) the relative rates of emergence of resistance to each of the three agents studied across the treatment arms, and (3) the effects of combinations of resistance mutations to these 3 classes of inhibitors on the viral drug resistance phenotype. These studies of HIV-1 resistance should provide important insights into the virologic explanation for the therapeutic success or failure of these combination regimens.